What is Osmoregulation? - How it effects salts and Water level in Blood?

Osmoregulation is the control of the levels of water and mineral salts in the blood. It is a homeostatic mechanism. There are three important homeostatic mechanisms: osmoregulation, thermoregulation and regulation of blood sugar levels. Homeostasis is important because it results in our cells being bathed in tissue fluid which has the correct amount of water, mineral salts, glucose and temperature.

A common misconception is that regulation of the plasma Na + concentration is closely correlated with the regulation of Na + excretion. However, it is related to volume regulation, which has different sensors and effectors (volume receptors) from those involved in water balance and osmoregulation (osmoreceptors).

The roles of these two pathways should be considered separately when evaluating patients. A water load, for example, is rapidly excreted (in 4-6 hours) by inhibition of ADH release. This process is normally so efficient that volume regulation is not affected and there is no change in ANP release or in the activity of the renin-angiotensin-aldosterone system. Thus, a dilute urine is excreted, and there is little alteration in the excretion of Na + . In contrast, the administration of isotonic saline causes an increase in volume but no change in plasma osmolality. In this setting, ANP secretion is increased, aldosterone secretion is reduced, and ADH secretion does not change. The net effect is the appropriate excretion of the excess Na + in a relatively iso-osmotic urine.

In some cases, both volume and osmolality are altered and both pathways are activated. For example, if a person with normal renal function eats salted potato chips and peanuts without drinking any water, the excess Na + will increase the plasma osmolality, leading to osmotic water movement out of the cells and increased extracellular volume. The rise in osmolality will stimulate both ADH release and thirst (the main reason why many restaurants and bars supply free salted foods), whereas the hypervolaemia will enhance the secretion of ANP and suppress that of aldosterone. The net effect is increased excretion of Na + without water.

This principle of separate volume and osmoregulatory pathways is also evident in the syndrome of inappropriate ADH secretion (SIADH). Patients with SIADH have impaired water excretion and hyponatraemia caused by the persistent presence of ADH; but the release of ANP and aldosterone is not impaired; thus, Na + handling remains intact. These findings have implications for the correction of the hyponatraemia in this setting and require restriction of water intake.

However, there is convincing evidence that ADH is also secreted by nonosmotic stimuli such as stress (e.g. surgery, trauma), markedly reduced effective circulatory volume (cardiac failure, hepatic cirrhosis), psychiatric disturbance, and nausea, irrespective of plasma osmolality. This is mediated by the effects of sympathetic overactivity on supraoptic and paraventricular nuclei. In addition to water retention, ADH release in these conditions promotes vasoconstriction owing to the activation of V1 (vasopressin) receptors distributed in the vascular tissue.